Some possible bearings of genetics on pathology

by Thomas Hunt Morgan

Fig. 12. Cross between hen-feathered Sebright cock and black-breasted game female belonging to a race with cock-feathered males. The offspring (F₁) are hen-feathered males and normal hens. These inbred give 3 hen-feathered to 1 cock-feathered son.

Now in this case we can perhaps go further. An examination of sections of the testes has shown that in the hen-feathered Sebright male there are certain kinds of cells, called luteal cells, while these are absent in the sections of the testes of normal cocks. These same luteal cells are like those present in the stroma of the ovary of all female birds. If we assume that they make an internal secretion that prevents the development of cock-feathering, both in the normal hen and in hen-feathered cocks, we have a complete explanation of all the facts. This explanation is made more probable by the results of removing the ovary of the hen, when, as Goodale has shown, the spayed hen develops the full male plumage of her breed. Since the luteal cells are present in the hen and in the hen-feathered cock, and are absent in the adult cock-feathered male, it seems not a far-fetched hypothesis to assume that these cells (or their secretions) are those involved.

The next illustration carries its into a more debatable field. Many human defects are connected with the nervous system, and it is interesting to find that many of them are believed to be inherited; even when no corresponding structural basis in the brain can be made responsible for the defect.

Feeblemindedness, insanity, and even some types of criminality have been said to be inherited according to a simple one-factor Mendelian difference. Owing to the difficulty of diagnosis it is obvious that the student of genetics would be expected to approach these problems with the utmost caution. The data, on which some rather sweeping conclusions have been based, sometimes show, on closer scrutiny, obvious contradictions. Take, for example, the case of feeblemindedness which has been represented as though it differed from the normal (whatever that may be) by a single Mendelian factor difference. The evidence for this is far from convincing, and all that can be safely said, I think, is that there are types of imbecility that may possibly be due to multiple factors, but until the relation of imbecility to various disorders of the glands and to syphilis has been thoroughly studied, even my cautious statement may seem to go too far. Curiously enough no one has as yet had the temerity to suggest that some of the high-grade imbecile types—the moron, for example—might represent an ancestral stage of the human race. If this were true, intelligence would then be looked upon as an innovation in the race, that has not yet spread to all of its members. I am aware that a similar suggestion has been made with respect to the criminal. Lombroso’s “criminal type” is notorious. The criminal has been painted as the ancestral brute from which the more docile human animal has arisen through loss of “wild-type” genes. I need not state, perhaps, that no one takes such speculations seriously today from a genetic standpoint.

Immunity and resistance to disease are subjects of great interest to geneticists as well as to pathologists.

Setting aside, of course, cases where the immunity is due to some temporary physiological state (little understood at present, I believe), and also setting aside immunity acquired by recovery from attack or inoculation, there still remain races that have, as we say, a constitutional resistance.

The best ascertained cases in this field are those worked out by Tyzzer and Tyzzer and Little. A carcinoma that originated in Japanese waltzing mice grew in practically every individual of the race when implanted. It failed to grow in “common” mice. The hybrid mice from these two races were also susceptible in nearly every case.

When the F₁’s were back-crossed to “common mice” the offspring were not susceptible. When the F₁’s were back-crossed to the Japanese waltzer all were susceptible. When the F₁’s were inbred only about 2.5 per cent. of the offspring were susceptible, [Fig. 13].